The autonomic nervous system (ANS) is part of the peripheral nervous system; it controls the activities of organs, glands and various involuntary muscles such as cardiac and smooth muscle. The ANS helps the body to adapt to changes in the environment and respond to stress. The ANS helps regulate: the size of blood vessels and blood pressure; the heart's electrical activity and ability to contract; the bronchium's diameter and thus air flow in the lungs.
The ANS affects heart rate, respiration rate, thermal regulation, digestion, salivation, perspiration, diameter of the pupils, urinary and sexual functions, metabolic and endocrine physiology.
The ANS acts through a balance of its two components, the sympathetic nervous system and parasympathetic nervous system.
The sympathetic nervous system (SNS) is involved in the stimulation of activities that prepare the body for action, such as increasing the heart rate, increasing the release of sugar from the liver, constricting blood vessels in organs not essential to fight or flight and other activities considered as fight-or-flight response.
The parasympathetic nervous system (PNS) activates resting functions, such as stimulating the secretion of saliva or digestive enzymes into the stomach and small intestine.
Generally, both sympathetic and parasympathetic systems target the same organs, but often antagonistically, e.g., the sympathetic system accelerates heart rate, while the parasympathetic system slows heart rate. Ordinarily, each system is stimulated appropriately to maintain homeostasis.
Autonomic failure, occurs when there is an imbalance between the sympathetic and parasympathetic divisions. Due to the many systems over which the autonomic nervous system exerts control, autonomic imbalance has manifold effects on the body, having serious cardiovascular, metabolic and endocrine consequences.
In particular, chronic sympathetic nervous system activation (SNS over-activity), plays a role in hypertension, Type II diabetes, obesity, metabolic syndrome and congestive heart failure. In essential hypertension, chronic sympathetic activation has been demonstrated to enhance cardiac myocyte growth, contributing to the development of left ventricular hypertrophy. In Type 2 Diabetes, chronic sympathetic activation contributes to increased insulin resistance and glucose intolerance.
Chronic sympathetic activation plays a significant role in cardiovascular disease. There is emerging evidence of a direct, causal linkage to the incidence of coronary heart disease clinical endpoints, such as myocardial infarction and sudden death and contribution of chronic sympathetic activation to mortality in congestive heart failure.
Chronic sympathetic activation is associated with clinical depression. The risk of heart attack has also been shown to be high in patients with depressive illness.
Obstructive sleep apnea (OSA) is associated with hypertension, Type II diabetes, obesity, metabolic syndrome, cardiovascular consequences including congestive heart failure and other endocrine consequences.
OSA is primarily characterized by sleep fragmentation and intermittent hypoxemia. The physiological stress imposed by the hypoxia and sleep fragmentation lead to a number of consequences including the direct effects of hypoxia and oxidative stress, hypothalamic pituitary adrenal dysfunction, systemic inflammation, changes in adipokine levels, disruption of sleep architecture and chronic sympathetic activation. Sympathetic activation in OSA, is a mediator of the causal link to the co-morbidities. OSA is a chronic slowly progressive disease that often may go undiagnosed for many years. In addition, the sympathetic activation seen in OSA may be present long before the OSA presents as clinically significant.
Current approaches to reducing sympathetic activation include weight loss, dietary calorie restriction and exercise. These approaches are typically unreliable, as they require behavioral modification and compliance can be low. Alternatively drugs may be used, including drugs that promote weight loss, e.g., sibutramine and antihypertensive drugs (e.g., beta-adrenergic drugs). Drugs acting on the central nervous system to reduce sympathetic outflow can be effective treatments for hypertension, but generally act non-specifically due to the broad interaction of the SNS and can have a high frequency of central nervous side effects and are generally not well tolerated by patients in long term therapy.
There is a need in the art for devices, systems, processor-readable media, and methods for inhibiting and/or reducing sympathetic activation through control and/or alteration of respiratory function.